CHEK1 and neoplasm: On the other hand, considering the overall high extent of ATM‐Chk2 and ATR‐Chk1 activation, we were surprised to find many tumours, particularly of the molecular subtype 3/4 (non‐Wnt2, non‐Shh), in which detectable p53 protein was limited to a very minor proportion (0.5–5%) of cancer cells (see Table 2).